POS0818 SOUTHEND PRE-TEST PROBABILITY SCORE AND HALO SCORE AS MARKERS FOR DIAGNOSIS AND MONITORING OF GCA: EARLY RESULTS FROM THE PROSPECTIVE HAS-GCA STUDY
Authors: A. Sebastian, A. Tomelleri, P. Macchioni, G. Klinowski, C. Salvarani, A. Kayani, M. Tariq, D. Prieto-Peña, E. Conticini, M. Khurshid, S. Inness, J. Jackson, K. Van der Geest, B. Dasgupta
Journal: Annals of the Rheumatic Diseases (2022)

Background Ultrasound (US) is recommended as the first line imaging test in patients with suspected Giant Cell Arteritis (GCA). Traditionally, the US halo sign has been used for diagnosis. We have recently described a composite Halo Score that allows to quantify vascular inflammation on US. Prospective studies on response and disease monitoring are lacking. Objectives To prospectively assess the role of US in diagnosing and monitoring GCA patients. We report early baseline and 12-month data on our current recruitment in a study that has suffered disruption from the pandemic. Methods HAS GCA (IRAS#264294) is an ongoing, prospective, multicentre study recruiting from referrals of suspected GCA to fast-track clinics. Based on the Southend GCA clinical pre-test probability score (SPTPS)1, patients were stratified in to low, intermediate and high risk categories2. Temporal and axillary US Halo Scores were calculated from the halo thickness and extent in bilateral temporal arteries, parietal and frontal branches (TAHS) and axillary arteries (AAHS). These scores were summed (TAHS x1 plus; AAHS x3) to generate a Total Halo Score (THS)3. Mann Whitney U test was used to compare baseline features between GCA and controls. Wilcoxon signed rank test was used to evaluate disease features at baseline and at 12 months in GCA patients. Sensitivity (Sn), Specificity (Sp) and ROC curve were calculated, where applicable. P value &lt;0.05 is statistically significant Results 202 patients (71 GCA, 131 controls) have been recruited thus far: 23 completed 12-month follow up assessment; 6 were lost to follow up (4 died, 2 withdrew consent due to pandemic). Demographics, clinical features, and US results are shown (Table 1). Table 1. Baseline features of GCA patients and controls GCA (n=71 ) Controls (n=131 ) P-value Age, median (IQR) 75 (70-81) 68 (62-76) 0.001 Female, n (%) 38 (54) 89 (68) 0.05 SPTPS category, n (%) Low risk 0 (0) 59 (45) &lt;0.001 Intermediate risk 16 (23) 49 (37) 0.04 High risk 55 (77) 23 (18) &lt;0.001 Halo score (HS), median (range) Temporal artery HS 12 (0-22) 2 (0-17) &lt;0.0001 Axillary artery HS 12 (0-21) 6 (0-18) &lt;0.0001 Total HS 21 (2-40) 8 (0-29) &lt;0.0001 Clinical features, n (%) Temporal headache 53 (75) 93 (71) 0.62 Scalp tenderness 36 (51) 40 (31) 0.006 Jaw claudication 38 (54) 9 (7) &lt;0.001 PMR symptoms 29 (41) 35 (27) 0.06 Constitutional symptoms 42 (59) 29 (22) &lt;0.001 Visual disturbance 40 (56) 58 (44) 0.11 Vision loss 21 (30) 9 (7) &lt;0.001 AA, axillary artery; GCA, Giant cell arteritis; TA, Temporal artery Among GCA patients, 50 had cranial, 5 large-vessel and 16 mixed phenotypes. Diseases were diagnosed by US and additional tests such as PET CT. Jaw claudication (54%) and constitutional symptoms (59%) were the dominant features in GCA patients. Median age was 75 years in GCA (54% females) and 68 years in controls (68% females). GCA and controls were stratified by SPTPS to Low risk (0% vs 45%; Sn-undefined, Sp-98), Intermediate risk (23% vs 37%; Sn-81, Sp-98) and High risk (77% vs 18%; Sn-98, Sp-91). Optimal SPTPS cut-off point was ≥12 (Sn-89, Sp-76). Median THS was 21 in GCA and 8 in controls. Optimal cut-off Halo Score in diagnosis was TAHS ≥5 (Sn-89, Sp-86), AAHS ≥11 (Sn-55, Sp-75), THS ≥15 (Sn-79%, Sp-86%). Baseline Halo Score and CRP levels showed positive correlation (spearman rank correlation). Among the 23 patients who completed 12-months follow up, median TAHS, AAHS and THS reduced from 12 to 2, 12 to 6 and 21 to 10, respectively (Figure 1). Conclusion Along with SPTPS, Halo Score successfully discriminates GCA from non GCA mimics and. HS is effective in showing 12-month response. This score may be a useful marker to monitor GCA disease activity References [1]Laskou F et al. Clin Exp Rheumatol. 2019 [2]Sebastian A et al. RMD Open. 2020 [3]Sebastian A et al. BMC Rheumatol. 2020 Disclosure of Interests Alwin Sebastian: None declared, Alessandro Tomelleri: None declared, Pierluigi Macchioni: None declared, Giulia Klinowski: None declared, Carlo Salvarani: None declared, Abdul Kayani: None declared, Mohammad Tariq: None declared, Diana Prieto-Peña: None declared, Edoardo Conticini: None declared, Muhammad Khurshid: None declared, Sue Inness: None declared, Jo Jackson: None declared, Kornelis van der Geest Speakers bureau: Roche, Grant/research support from: Mandema stipend, Bhaskar Dasgupta: None declared